CHEMICAL AGENTS AS WEAPONS: MEDICAL IMPLICATIONS

CHEMICAL AGENTS AS WEAPONS: MEDICAL IMPLICATIONS

BY KEN MILLER, M.D., Ph.D.

Many common chemicals can produce unpleasant symptoms or injuries. Most victims of attacks involving chemical agents will be treated according to their symptoms. The most important intervention is decontamination of the exposed victims, which will prevent the victim from further absorbing the agent and will prevent secondary contamination of rescuers. If high explosives are used to disperse the agent, traumatic and blast injuries will also be present.

Some of the differences between a terrorist haz-mat incident and other multivictim incidents and triage scenarios are the following: (1) recognizing early in the incident that there has been exposure to some sort of chemical, (2) gaining safe access to and rescue of nonambulatory victims, and (3) establishing a decon corridor for ambulatory and nonambulatory victims.

DISPERSION

Inhalation is the most rapid means of absorbing chemical agents, but unlike biological agents, they can also be absorbed across the skin and mucous membranes. Chemical agents can be effectively dispersed as a gas, vapor, liquid, or solid from something as simple as an open container. The effectiveness of the method of dispersion depends on such physical properties as vapor pressure, boiling point, and vapor density, as well as climatic conditions.

Dispersion may also be by vaporization within or in close proximity to a forced ventilation system or by a high-explosive device.

One observation that should raise the suspicion that an explosive device was used to disperse a chemical or biological agent is a small explosion that otherwise seems to do little damage. If there are no apparent antipersonnel fragmentation, incendiary, or strategic structural destabilizing effects, consider that the purpose of the blast might have been to spread some substance around. So, be wary of small explosions.

Other indications that an attack may have a more sinister purpose might be the location and timing of the assault. High-profile government, political, religious, and sporting events would be expected to attract a terrorist`s attention.

Dispersion of a chemical agent indoors vs. outdoors will affect the atmospheric concentration and exposure time of the victims–major determinants in the severity of subsequent toxicity. Favorable climatic conditions are nighttime (ultraviolet light can slowly destroy some biological and chemical agents), cool temperature, and minimal wind (reducing the rate of dissipation and keeping any aerosol or vapor closer to the ground).

DETECTION

Realistically, the only likely detection method available to the first-arriving companies, short of a preincident phone call to tip off the press or other parties, will be circumstantial evidence.

As always, respiratory protection with SCBA and structural turnout gear should be the basic protection. This level of protection may be sufficient for light contamination, dissipated vapor or gas, and very short exposure time. Immediate decontamination of personnel with water after short life-saving entries will reduce the risk of significant exposure. Level A haz-mat protection would be the safest personal protection for investigation, surveillance, and rescue. This type of protection takes time to implement and would likely not be an option for the first-in assignment.

It may not be possible to know that the situation is a potential haz-mat incident, however, until the initial interior size-up has been completed. Once this possibility is recognized, tactical withdrawal and immediate decon should reduce the risk of further exposure.

Another way to identify a potential haz-mat incident is to assess the symptoms of victims exiting the targeted site or structure. Some indicators that the situation is likely to be a toxicological multivictim incident would be victims` eye, upper airway, or pulmonary symptoms; unfamiliar odors; or fairly rapid incapacitation. In such circumstances, entry into the incident site would be limited only to very brief specific life-saving missions such as immediate drag and rescue of visible unentrapped nonambulatory victims. This would then be followed by emergency decon of both the victims and rescuers.

The syndrome of mass psychogenic illness is common at high-profile hazardous-materials incidents, and the resulting vague but very real (to the victim) symptoms can further tax responders` resources. It has been suggested that separating the uninjured noncontaminated evacuees from triage areas and staging areas and out of sight of the field of operations will reduce the number of collateral acute anxiety reactions. Symptoms of this nature tend to be spread by the incident`s sights and sounds.

DECONTAMINATION AND TRIAGE

The challenge will be to set up immediate decon for the exiting ambulatory victims before they self-triage to local hospitals and contaminate or incapacitate these resources. The best strategy is to preplan tactics expecting that the identity of the specific chemical or biological hazard will not be known until much later in the incident.

As already indicated, decontamination is the key to success in incidents involving chemical agents. It is reasonable to expect–regardless of whether exposure is through inhalation, skin, or mucous membrane absorption–that rapid decon should reduce some of the toxicity risk.

Levels of Decon

Several levels of decon will have to be considered:

Victim decon–ambulatory, nonambulatory, and deceased. This may involve the decon of a large number of victims.

Technical decon of Level A or B protection rescuers and equipment after victim rescue and victim decon procedures.

Emergency decon of acutely symptomatic victims or rescuers with a breach of personal protective equipment or who may have made initial entry in structural protective gear and SCBA.

Decontamination represents a problem from the very beginning of the incident. How does the need for decon affect the way we perform multivictim incident (MVI) or mass casualty incident (MCI) triage? Using START (simple triage and rapid treatment), all ambulatory victims are identified quickly, led off-site, and then individually triaged. This may be a bit more challenging in real life than in practice, as victims scatter from the hazard.

The nonambulatory victims are then triaged on-site as “immediate” or “delayed,” according to RPM (respiration, perfusion, and mental status). This simple and familiar approach requires contact and communication with the victims.

The ambulatory victims can be led to a decon corridor of sequential elevated fog-pattern master streams and instructed to undress under tarps hung between apparatus (secure the clothing; it is evidence), wash again (maybe assisted by gender-specific firefighters), and redress in large plastic garbage bags (which are cheap and available–obviously not clear ones). They then are entered into START triage. Keep in mind that wound irrigation with saline is part of the decon process.

You can imagine two things here: This system has to be set up and run efficiently to be effective (that`s why it`s essential to keep it simple). Some victims–such as the elderly, individuals with special medical needs, those with evolving serious injury evident only after some walking, and some children–may not be able to follow these steps and will need to be reassigned to be deconned with the nonambulatory victims.

Nonambulatory victim decon can proceed by systematically removing clothing by cutting the front and rolling the cloth back; washing with water or soap and water (in two stages, if heavily contaminated), paying attention to body creases; and drying.

A diluted bleach solution (1:10, 0.5%) is an option for skin and equipment decon (not for wound or eye decon) but may not be routinely available. This has been suggested because hypochlorite oxidizes organics and kills biologicals. However, these effects depend on contact time and are not a priority.

This operation should be done in Level B or possibly Level C protection. Initially, it may have to be done in structural gear and SCBA (duct-tape the neck, waist, wrists, and ankles for added protection if crews are rotated and are regularly deconned themselves).

Emergency decon has two critical functions: (1) to decon victims who are judged to be able to survive but who require advanced life support (ALS) and (2) to decon the first-in assignment firefighters who were exposed to the hazard without Level A or Level B protection during initial rescue and size-up.

Medical Intervention

As with any other MCI, the level of medical intervention will depend on the number of victims and EMS resources available. Generally in an MCI, medical intervention is limited to first aid and transport. ALS may not be practical, but decon will still be needed. In smaller incidents, ALS may be possible, and even desirable, when resources are available. This raises the questions of how to triage given the added problem of victim contamination and when to attempt definitive medical interventions during the decon process.

One reasonable approach to pre-decon triage is to identify and decon ambulatory victims first, conscious nonambulatory victims next, followed by unconscious nonambulatory victims, then the deceased. This is contrary to the priorities of START, but it is workable when the number of victims greatly exceeds the resources immediately available. When fewer victims are involved and resources are reasonably available, the START triage followed by decon of the immediate category, the delayed category, and then the minor category is possible. Some of these triage categories will be ambulatory; some will not. Setting up parallel ambulatory and nonambulatory decon will speed this process and minimize the victim self-triage rate. In the true mass-casualty situation, when resources are grossly inadequate, we are trying to provide the most resources to the most survivable victims. In smaller incidents, we maximize therapy to those in greatest need. These are quite opposite concepts; the one chosen will depend entirely on the balance between victims and resources. If START is used, respiration counting, perfusion by capillary refill, and mental status should be possible to assess while in Level A protection.

Life-Saving Interventions

When ALS is attempted, some interventions may be tried before decon, during decon, and after decon. After decon is completed, we are back to operations as normal and can proceed with standard tactics. Sometimes critical interventions will be necessary before decon is started or completed. The most likely life-saving interventions will be establishing an airway and assisting ventilation, needle thoracostomy to decompress a tension pneumothorax, and control of exsanguinating hemorrhage. Occasionally a specific antidote–such as atropine in organophosphate or nerve agent poisoning or nitrites and thiosulfate in cyanide poisoning–will also be life saving.

The vast majority of hazardous-materials exposures will be managed symptomatically with emphasis on respiratory and airway management, multisystem traumatic injury, eye injury, chemical burns, and changes in mental status. If life-saving interventions are to be attempted before decon, one approach to reducing secondary rescuer contamination is to wrap the victim in a tarp, allowing only the head to be exposed, so that airway management and assisted ventilation are possible. Once out of the hazard area, it may be possible to perform these functions in Level B protection.

In the case of nerve agent exposure, atropine can be given intramuscularly instead of intravenously before or during decon. Atropine can still be effective by this route, and this technique is technically easier to use while in protective gear.

The key strategy if attempting ALS interventions before decon is to minimize the effect on victim flow through the decon corridor by reducing their triage acuity and buying time for effective decon. If an acute problem can be satisfactorily managed before or during decon, the impact on decon priority will be less, and victim flow will go more smoothly.

NERVE AGENTS

To keep this discussion manageable, the nerve agents are used as a model of the chemical agents. (Other agents are briefly discussed on page 68.) Highly toxic, they demonstrate many principles of hazardous-materials management, have specific therapies, and have been used in an urban environment. Many important lessons have been learned from incidents involving their use.

Nerve agents are extremely potent organophosphates, as are the commercial pesticides. These agents have volatility ranges from that of water to that of motor oil. Nerve agents are mostly clear, colorless, and odorless liquids at ambient temperatures and have fairly high vapor densities. They cause their biological effects by inhibiting the enzyme acetylcholin-esterase, which allows the chemical acetylcholine to accumulate in various muscles, nerves, and glands, resulting in hyperactivity. Death is caused by respiratory failure and seizures.

Symptoms

The symptoms of nerve agent poisoning in part depend on the route of exposure. When exposure occurs by vapor, the eye is the first organ to be affected. Symptoms will include pinpoint constricted pupils, blurred vision, inability to focus, tearing, and pain.

Upper respiratory symptoms of runny nose and lower respiratory symptoms of labored respiration, productive cough, wheezing, and increased pulmonary secretions follow. All these symptoms can manifest themselves fairly immediately after vapor exposure.

Liquid exposure on the skin may delay the onset of symptoms, since absorption is a little slower. Depending on the quantity of the agent involved, there could be a several-hour delay in symptom onset. Early symptoms here might be sweating and muscle twitching at the site of exposure followed by nausea, vomiting, and diarrhea. Progression to respiratory symptoms may also occur. After exposure to a large quantity of agent by either route, the predominant symptoms are loss of consciousness, seizures, sudden and severe pulmonary edema, apnea, and death.

Therapeutic Options

Unlike most chemical agents, there are therapeutic options to treat nerve agent poisoning. The treatment strategy is first to block the effects of excessive amounts of acetylcholine with atropine and then to regenerate the enzyme acetylcholinesterase with pralidoxime (PAM). When given soon after symptoms begin to appear, atropine can block the effects of the excessive acetylcholine. The respiratory system is the primary organ system to benefit from atropine. The runny nose, labored breathing, excessive secretions, and wheezing will improve. These are also the most dangerous early symptoms of moderate exposure to nerve agents. The more severe symptoms, such as seizures and muscular weakness leading to paralysis, will not respond to atropine. Seizures are treated with diazepam (Valium) or a similar drug depending on local protocols.

There is no direct antagonist for the muscle weakness, however. Instead, the treatment is to administer pralidoxime to regenerate the enzyme acetylcholinesterase by releasing the bound nerve agent. The problem here, however, is that the chemical bonding of the nerve agent with the enzyme (aging) occurs faster with some nerve agents than with others. Those nerve agents that age more quickly would have to be treated sooner with pralidoxime to reverse the process. Once the nerve agent and the enzyme have covalently bonded, return to normal enzyme activity depends on the body`s synthesis of new enzyme, which, of course, takes time.

Therefore, in the more severe cases of nerve agent poisoning, muscle weakness or paralysis may persist longer than the eye, pulmonary, and gastrointestinal effects. If the respiratory muscles are affected, assisted ventilation may be needed for a prolonged period of time. The eye effects of nerve agent poisoning are least responsive to atropine. Fortunately, they are not dangerous and will improve over time.

Of all the treatment options for nerve agent poisoning, those most likely to be life-saving will be early decon, aggressive airway management, atropine for pulmonary edema and wheezing, and diazepam for seizures.

Preventing Symptoms

Some symptoms of nerve agent poisoning can be prevented before exposure has occurred or symptoms have progressed too far. The military has used the drug pyridostigmine (Mesthinon) to pretreat soldiers likely to encounter a nerve agent attack. This drug works in the same way as the nerve agents themselves by inhibiting the enzyme acetylcholinesterase, but it does this reversibly. It ties up some of the enzyme, preventing it from binding with the nerve agent and producing symptoms like those of mild nerve-agent poisoning. These symptoms, however, are not incapacitating, and the soldier can still carry out the mission. Of course, if the soldier is exposed to a nerve agent, he will have to be deconned just as anyone who has not been pretreated, but less antidote or no antidote may be needed. Clearly, this tactic is not practical for the fire service, since exposure may never occur (we hope), and side effects of pretreatment would be unacceptable. It takes some time for pyridostigmine to work, so pretreatment at the time of the incident is not practical.

What may be important to us, though, is self-treatment or buddy treatment with intramuscular atropine if mild to moderate symptoms develop during rescue or decon operations. Intramuscular atropine can prevent symptom progression as long as further absorption does not occur and the exposure is minimal.

There are some considerations with this approach. Atropine itself causes dry mouth and may cause drowsiness or confusion at higher doses. More importantly, because it reduces sweating, atropine will predispose the firefighter to heat exhaustion or heat stroke. This is a major consideration for personnel working in Level A protection and may require affected personnel to rotate out of that position and assume duties where they can be regularly monitored, placed in rehab for observation, or transported offsite if still symptomatic. n

References

Medical Management of Chemical Casualties Handbook, Chemical Casualty Care Office, Medical Research Institute of Chemical Defense, 2nd edition, Sept. 1995.

“Proceedings, Conference on Lifesaving Intervention,” National Disaster Medical System, Denver, 1998.

Field Operations Guide, Metropolitan Medical Strike Team, U.S. Department of Health and Human Services, Office of Emergency Preparedness, Rockville, Md.

Intensive Care Medicine 21:1032, 1995.

American Journal of Emergency Medicine 15:527, 1997.

Annals of Emergency Medicine 28:129, 1996.

Annals of Emergency Medicine 28:223, 1996.

Annals of Emergency Medicine 21:303, 1992.

Common Chemical Agents

Nerve agents: GA (tabun), GB (sarin), GD (soman), GF, VX.

Antidotes to consider: atropine, diazepam (Valium), pralidoxime (2-PAM).

Vesicant (blister agents): sulfur mustards (HD, H), L (Lewisite), CX

(phosgene oxime).

Cyanides (blood agents): AC (hydrocyanic acid), CK (cyanogen chloride).

Antidotes to consider: amyl nitrite, sodium nitrite, sodium thiosulfate.

Pulmonary agents: CG (phosgene), chloropicrin (PS), chlorine, isocyanates.

Riot control agents: CS, CN (MaceTM), CR, capsaicin oleoresin (pepper spray).

Additional Nerve Agents

SARIN ATTACKS

In June 1994 and again in March 1995, Japan experienced two major urban peacetime terrorist haz-mat events. Both events involved the nerve agent sarin (GB). The first incident was an attack on a residential area in Matsumoto. It was reported about midnight and ultimately resulted in approximately 600 exposed casualties, 58 hospitalizations, and seven deaths.

The initial dispatch was as a residential odor of gas. The identity of the agent was not known at the time of dispatch, nor was it determined during the incident. Sarin was identified seven days later through air, water, and soil analyses. No decon was attempted or considered necessary, since no causative agent was evident during the incident. Decon was not considered at the hospitals.

Eight responders and an unreported number of hospital personnel experienced mild symptoms of nerve agent exposure. None were disabling, none were treated, and all symptoms were self-limited.

Tokoyo

The experience in Matsumoto played out again on a large scale in Tokyo less than one year later. At approximately 8 a.m. on a Monday during rush hour, sarin was released by passive evaporation from open containers in five subway cars on three subway lines. No effort was made to disperse the agent actively. The initial call for help was for a gas explosion in the subway. There were 11 fatalities and 5,000 evacuees.

From subsequent reports, about 540 people sought medical attention at the nearest hospital. Of these, 64 were transported by ambulance and 35 by public safety vans. This left 441 people who self-triaged to the nearest hospital. That`s more than an 82 percent self-triage rate. This hospital reported that 82 percent of this patient load was eventually discharged from the emergency department and 18 percent was admitted (most patients were discharged in two to four days). They had two of the 11 fatalities and received two victims in respiratory arrest, who were subsequently resuscitated.

The first victims began arriving about one-half hour after the emergency call to the subway. The most severe symptoms were respiratory, requiring intubation and assisted ventilation (total of five including the two mentioned in respiratory arrest). All of these victims initially complained of eye symptoms before respiration became compromised. Moderate symptoms were weakness, labored breathing, muscle twitches, and seizures. None of these victims required respiratory assistance. Mild symptoms were dilated pupils, eye pain, dim vision, and decreased visual acuity. These victims were observed and discharged from the emergency department.

Ninety-six percent of the moderate to severe victims were treated with atropine and pralidoxime; only 19 percent of those treated required more than 2 mg of atropine. Diazepam was given to eight victims for seizures. Acute stress disorder was reported in 33 percent of victims reporting to this hospital (some type of symptoms but judged not consistent with nerve agent poisoning). All treatment was based on the symptoms presenting and the prior experience in Matsumoto.

Sarin was not identified as the causative agent until six hours into the incident. No decontamination was performed other than for clothing removal. Since the exposure was by means of a vapor, this might seem reasonable; however, offgassing of vapors caused hospital personnel to experience mild symptoms.

Another report about the Tokyo incident attempted to relate the occurrence of symptoms in receiving hospital personnel. These authors found symptoms such as dim vision, runny nose, labored breathing, chest tightness, cough, dilated pupils, and increased salivation. Those who performed CPR or removed victims` clothing reported the most symptoms. All hospital personnel were able to continue working, but some were treated with 0.5 to 1 mg of atropine.

The medical staff noted an odor on the most symptomatic victims as they arrived, but it was not until the hospital staff began to experience symptoms that the need for some form of decon was recognized. Even then, decon consisted only of removing clothing and storing it outside of the hospital and forced ventilation of the emergency departments.

This information about victim and hospital personnel symptoms would be vital to the incident commander working a possible terrorist haz-mat incident. It will help him to gauge the hazards to rescue personnel, decon level requirements, and scene medical treatment options.

This reverse flow of information from receiving hospitals to incident command is not common. Other hospitals would also benefit from this information for planning pre-triage decontamination of self-transporting victims. It is interesting to note that despite the fact that all victims were exposed to sarin vapor only, there were still secondary effects on personnel coming in contact with them. Had the victims been contaminated with liquid product, secondary contamination would have been much more severe without the implementation of field or hospital decon.

VESICANTS

This group includes the sulfur mustards (named for their odor), the trivalent arsenic agent Lewisite, and phosgene oxime. The most important thing to note here is that vesicants have a delayed onset of symptoms. These agents chemically alter cellular enzymes, proteins, and DNA. They damage cells of the skin and mucous membranes on contact, but this damage takes time to show up. Several hours after contact, blisters develop, and a chemical burn becomes the primary injury. Lewisite and phosgene oxime produce immediate pain, but the mustards may cause only a little redness similar to that of an early sunburn and can easily be overlooked. Immediate skin and eye decon are essential. Pay special attention to areas such as the neck, groin, and axillae, where vapor or liquid can be held in the skin moisture.

Deaths result from inhalation, where sloughing of damaged mucous membranes obstruct airways, causing hypoxia. It is also possible that if enough skin surface is exposed to these agents, the resulting burn injury can lead to fluid loss, shock, organ failure, and sepsis leading to death.

These agents also have delayed effects on the blood-forming elements of the bone marrow, leading to reduction in all blood cells, anemia, and sepsis.

Aside from decon, treatment is aggressive airway management and, later, burn wound care. Lewisite, the arsenic-containing agent, has a specific treatment with a chelating agent called “BAL” (British Anti-Lewisite, dimercaprol).

CYANIDES

Although cyanides are extremely toxic when inhaled or ingested, hydrogen cyanide gas is less dense than air and easily dissipates. They do not make good chemical warfare agents because the gas does not stick around long enough to generate sufficient concentration-time thresholds. However, on a smaller scale, food sabotage or an indoor release could still be a problem. One reported form of booby trap involving cyanide is the clandestine meth (methamphetamine) lab “security”–a dish of sodium or potassium cyanide with a bottle of acid propped nearby so that anyone entering will dump the acid onto the salt, forming hydrogen cyanide gas. This could be one of many hazards during meth lab takedowns or fire suppression responses. By the way, cyanide is a combustion product of acrylonitrile plastics and is believed to be an important factor, along with carbon monoxide, in smoke-inhalation injury.

Cyanide inhibits the chemical chain reaction that allows cells to use oxygen. So even though breathing may be adequate, or even if breathing is assisted, the cells cannot use the available oxygen, and marked acidosis results. This is one situation where the pulse oximeter may show normal or near-normal hemoglobin saturation with oxygen while the victim may still be in serious trouble. Even though oxygenation is adequate, the cells can`t pick up and use the oxygen from the hemoglobin.

The antidotes used here are pretty clever. First, inhaled amyl nitrite or intravenous sodium nitrite is used to convert some of the hemoglobin in blood to a form that can carry cyanide away from the tissues (oxyhemoglobin to methemoglobin to cyanomethemoglobin). Then intravenous sodium thiosulfate is given to provide sulfur to the liver, which can convert cyanide to nontoxic thiocyanate (by the enzyme rhodanese), which can be excreted by the kidneys.

PULMONARY (CHOKING) AGENTS

Organohalides, chlorine, oxides of nitrogen, and phosgene cause upper airway symptoms and noncardiogenic pulmonary edema. The catch is that there can be a delay of up to 24 hours in the onset of systems postexposure. Treatment is supportive, including supplemental oxygen, bronchodilators like albuterol, positive-pressure ventilation, and endotracheal intubation.

The usual drugs for pulmonary edema due to heart failure like nitroglycerine, morphine, and furosemide (Lasix) will not work for this noncardiogenic form of pulmonary edema. The problem is capillary leak within the lungs due to the chemical injury, not heart failure and the building up of backpressure into the lungs.

RIOT CONTROL AGENTS

These agents are solids dispersed in fine particles or in solution. They cause pain and irritation to mucous membranes and skin. They cause tearing of the eyes, eyelid spasm, runny nose, cough, and eye and skin pain and redness. Occasionally, they may provoke underlying asthma or chronic obstructive pulmonary disease, but this is unusual.

Treatment is irrigation (while standing upwind) and bronchodilators, if needed, for wheezing. When capsaicin oleoresin (pepper spray) is involved, luminum- or magnesium-containing liquid antacids have been used on the skin to relieve pain. n

Editor`s note: Dr. Miller discussed biological agents in “Biological Agents as Weapons: Medical Implications,” Fire Engineering. January 1999.

n KEN MILLER, M.D., Ph.D., is medical director of the Orange County (CA) Fire Authority, medical team manager of USAR CA TF-5, and unit commander of DMAT CA-1. He is also an assistant professor of emergency medicine at the University of California-Irvine Medical Center. He formerly spent 13 years as an EMT-B and paramedic for the Exeter Township (PA) Ambulance Association, Hershey (PA) Fire Department, Mercy Ambulance (Las Vegas), and San Diego City Paramedic Services. He has a B.S. in chemistry and a Ph.D. in pharmacology and is a board-certified emergency physician.

No posts to display